The objective of this study was to evaluate whether the oxidative stress caused by aluminum (Al) toxicity is an early symptom that can trigger root growth inhibition in Macaca (Al-sensitive) and SMIC148-A (Al-tolerant) potato clones. Plantlets were grown in a nutrient solution (pH 4.00) with 0, 100 and 200mg Al L(-1). At 24, 72, 120 and 168h after Al addition, root length and biochemical parameters were determined. Regardless of exposure time, root length of the Macaca clone was significantly lower at 200mg Al L(-1). For the SMIC148-A clone, root length did not decrease with any Al treatments. Al supply caused lipid peroxidation only in Macaca, in both roots (at 24, 72, 120 and 168h) and shoot (at 120 and 168h). In roots of the Macaca, catalase (CAT) and ascorbate peroxidase (APX) activity decreased at 72 and 120h, and at 24, 72 and 120h, respectively. At 168h, both activities increased upon addition of Al. In roots of the SMIC148-A, CAT activity increased at 72 and 168h, whereas APX activity decreased at 72h and increased at 24, 12 and 168h. The Macaca showed lower root non-protein thiol group (NPSH) concentration at 200mg Al L(-1) in all evaluations, but the SMIC148-A either did not demonstrate any alterations at 24 and 72h or presented higher levels at 120h. This pattern was also observed in root ascorbic acid (AsA) concentration at 24 and 120h. The cellular redox status of these potato clones seems to be affected by Al. Therefore, oxidative stress may be an important mechanism for Al toxicity, mainly in the Al-sensitive Macaca clone.